We propose research on the effects of coronary artery ligation on vascular permeability and blood-interstitium-lymph exchange in the lungs in the absence of significant left-ventricular dysfunction. Patients with acute myocardial infarction can develop the signs of pulmonary edema in the absence of heart failure. We hypothesize that coronary ishemia and infarction may initiate events which can lead to increased microvascular permeability in the lungs and contribute to development of pulmonary edema before pressure rises in the lung vasculatue. We propose to study these effects in anesthetized sheep. Branches of the anterior descending coronary artery will be ligated. Lung blood-tissue-lymph transport will be documented by measuring lung lymph flow, plasma and lymph protein content, pulmonary arterial and left atrial pressures, and 3HOH extravascular volume and 14C-urea permeability surface area product by a multiple-tracer technique. The influence of the following variables will be measured: 1) the degree of myocardial flow reduction as varied by altering the site of occlusion and documented by labelled microspheres; 2) the effects of elevating left atrial pressure by balloon obstruction of the mitral valve combined with coronary occlusion. In addition, an exploration of the mechanism for lung vascular permeability increase will be sought by the infusion of blockers of adrenergic action, antihistamines, blockers of prostagandin synthesis and by granulocyte depletion. The results should provide insight into the importance of the linkage between coronary ischemia and lung microvascular exchange. This information is relevant to the early treatment and management of the complications of myocardial infarction.